Most models of insomnia hypothesize an individual predisposition to the disorder along with precipitating factors. Converging evidence suggests exposure to stressful life events can precipitate insomnia. However, research has yet to identify a trait predisposition to insomnia, or investigated the interaction of stress exposure with that predisposition. The purpose of this study is to prospectively determine the importance of sleep reactivity (i.e., non-insomniac individuals who reliably exhibit sleep disruption in response to stress) for the development of chronic insomnia following naturalistic exposure to stressful life events. We have developed and validated a measure of sleep reactivity that in normal individuals is predictive of 1) polysomnographic sleep disturbance in response to laboratory stressors and 2) the prospective development of insomnia over a 13-month follow-up period. It is hypothesized that normal sleeping individuals without a history of insomnia who have a high premorbid sleep reactivity will be at greater risk (i.e., predisposed) to developing chronic insomnia following exposure to stressful life events when compared to individuals with low sleep reactivity. Prospective data will be collected from 2,200 individuals without insomnia regarding their experiences of stressful life events and insomnia incidence during a 2-year assessment period. It is hypothesized that these two factors will have a greater than additive effect in predicting insomnia incidence (i.e., exposure X predisposition interaction). The predictive value of laboratory measured sleep reactivity in predicting insomnia incidence will also be determined in a randomly selected subset of individuals over a 4 year follow up period. Identifying and following individuals who are likely to develop insomnia will allow the study of phenotypic traits characteristic of insomnia prior to the development of the disorder, improve our limited understanding of its temporal course and its association with morbidity, help identify specific triggers and their impact in at-risk populations, and permit efforts to be directed toward prevention rather than treatment.